[A case of Achilles tendon rupture in a patient of refractory Reiter's syndrome].

We herein report a case of spontaneous rupture of Achilles tendon in a 51-year-old man with refractory Reiter's syndrome. On the diagnosis in November, 2006, physical examinations and MR images showed a remarkable inflammation at the calcaneal insertion area of Achilles tendon. He required aggressive treatments with nonsteroidal anti-inflammatory drug (NSAID), oral prednisolone 30 mg daily and methotrexate (8 mg weekly) to control the disease. Two months later, the Achilles tendon ruptured at its insertion point. This ruptured lesion of Achilles tendon was an unusual site compared to previous reports. Histological findings in the ruptured lesion of Achilles tendon revealed the existence of granulomatous lesion consisted of severe infiltration of fibroblasts and vessels proliferation beside tendon. These findings suggest a prolonged inflammation. Although it is widely accepted that Reiter's syndrome is associated with enthesis, especially at the attachment of Achilles tendon to calcaneum, there have been only two reports of Achilles tendon rupture associated with Reiter's syndrome. The possible cause of the Achilles tendon rupture in this patient might be due to the weakened strength of the Achilles tendon by the prolonged and severe enthesis of Achilles tendon near the insertion lesion.

Role of sphingosine 1-phosphate in the pathogenesis of Sjögren's syndrome.

Primary Sjögren's syndrome (SS) is an autoimmune disease characterized by inflammatory mononuclear cell infiltration and destruction of epithelial cells of lacrimal and salivary glands. Sphingosine 1-phosphate (S1P) and signaling through its receptor S1P(1) have been implicated in many critical cellular events including inflammation, cancer, and angiogenesis. This study was undertaken to examine the role of S1P(1) signaling in the pathogenesis of primary SS. S1P(1) and sphingosine kinase 1, which converts sphingosine to S1P, were detected in the cytoplasm of inflammatory mononuclear cells, vascular endothelial cells, and epithelial cells in all labial salivary glands by immunohistochemistry. The expression of S1P(1) in inflammatory mononuclear cells was enhanced in advanced stages of primary SS. S1P enhanced proliferation and IFN-gamma production by CD4(+) T cells. The enhancing effect of S1P on IFN-gamma production by CD4(+) T cells was stronger in patients with primary SS than in healthy controls. S1P also enhanced Fas expression and Fas-mediated caspase-3 induction in salivary gland epithelial cells. IL-6 expression was detected in the cytoplasm of inflammatory mononuclear cells and ductal epithelial cells and was enhanced in advanced stages of primary SS. Furthermore, both IFN-gamma and S1P augmented IL-6 secretion by salivary gland epithelial cells. These effects of S1P were inhibited by pretreatment of pertussis toxin. Our data reveal that S1P(1) signaling may modulate the autoimmune phenotype of primary SS by the action of immune as well as epithelial cells.